Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The observation that suckling evokes a modest rise in serum TSH when compared with that of prolactin is inconsistent with the hypothesis that TRH serves as a hypophysiotropic mediator of this response. In the present study we attempted to provide an explanation for this discrepancy by determining whether any of a growing number of putative prolactin releasing factors could alter pituitary responsiveness to TRH. Anterior pituitaries from lactating (day 14) rats were monodispersed with trypsin, cultured for 2 days, and then incubated in the presence of medium alone or medium containing TRH, dopamine, or a combination of these secretagogues. Companion sets of cultures were incubated concurrently with either beta-endorphin, neurotensin, oxytocin, serotonin, vasoactive intestinal polypeptide, or lysine vasopressin. As expected, TRH stimulated and dopamine suppressed prolactin release. None of the substances tested except oxytocin had a significant effect on pituitary cell responsiveness to TRH or dopamine. Oxytocin had no effect on prolactin secretion when tested alone or in combination with TRH and dopamine. TRH alone stimulated TSH release by these cultures, while oxytocin and dopamine were ineffective by themselves. However, TSH secretion by cultures treated simultaneously with TRH and oxytocin could be suppressed to approximately half of that released by cells incubated with TRH alone. These results demonstrate that oxytocin attenuates TRH-induced TSH release by a direct action on pituitary cells without affecting the prolactin response. This selectivity of responsiveness imparted by oxytocin might contribute to the blunted release of TSH after suckling.
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PMID:Oxytocin attenuates TRH-induced TSH release from rat pituitary cells. 315 75

Oxytocin (OXY) and arginine-vasopressin (AVP) are widely distributed within the brain and have a number of behavioral effects resulting from central administration. We have previously found that central OXY administration accelerated the onset of maternal behavior in ovariectomized (OVXed) estrogen-treated nulliparous rats. We now report that intracerebroventricular (ICV) injections of OXY enhance lordosis behavior in OVXed estrogen-treated rats. After treatment with 0.15, 0.20, or 0.25 micrograms EB IM for three days, OXY (800 ng) infusion ICV on the fourth day produced a significant increase in lordosis behavior between 20 and 90 minutes after administration. Doses of OXY between 0.8 and 5 micrograms injected ICV significantly increased lordosis behavior in animals pretreated with 0.5 micrograms EB for three days. In other OVXed rats treated with 0.5 micrograms EB for three days, ICV injections of 1 micrograms OXY or an equimolar dose of AVP significantly increased lordosis while equimolar doses of ACTH1-10, ACTH4-10, arginine-vasotocin, GnRH and alpha-MSH did not significantly increase lordosis behavior over saline vehicle levels. ACTH1-24 significantly lowered lordosis quotients. We have concluded from these data that central administration of OXY (and possibly AVP) enhance female sexual receptivity. This effect is estrogen dependent, dose related and under our test conditions, specific to OXY and AVP.
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PMID:Oxytocin facilitates the sexual receptivity of estrogen-treated female rats. 370 83

Of the primary neuronal tissue cultures (glia cell, neuronal cells, mixed and retina cultures), the neuronal cells of (cells + medium) display the highest total porphyrin production from 10(-3) M delta-aminolaevulinic acid (ALA). In the presence of 10(-3)-10(-6) M melatonin, the quantity of total porphyrins produced by the neuronal cultures decreases in inverse proportion to the concentration. Oxytocin, lysine-vasopressin, CCK-8 sulphate ester and des-Tyr-gamma-endorphin in concentrations of 10(-5) and 10(-6) M block the porphyrin synthesis of the glia cells and display different effects on that of the neuronal cells. They enhance the total porphyrin synthesis of the cell cultures, with the exception of 10(-5) M des-Tyr-gamma-endorphin, which exerts an inhibitory effect on the glia cells.
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PMID:Porphyrin synthesis in primary nervous tissue cultures from 10(-3) M delta-aminolaevulinic acid in the presence of melatonin and neuropeptides. 372 65

The intracerebroventricular (i.c.v.) injection of oxytocin, in doses ranging from 5 to 90 ng (5-90 pmol) induced penile erection and yawning in male rats. Such response was not induced by doses of the peptide higher than 100 ng, nor by equimolar doses of i.c.v. [Arg8]vasopressin, ACTH-(1-24), alpha-MSH, rat corticotropin-releasing factor (rCRF), delta sleep-inducing peptide, neurotensin or substance P. Oxytocin-induced penile erection and yawning were prevented by atropine and morphine, but not by methylatropine or the opiate antagonist naloxone. Haloperidol, a dopamine receptor antagonist, was ineffective at low doses; it partially prevented penile erection but not yawning at high doses. Since oxytocin is present not only in the neurohypophysis but also in other brain areas, our results suggest that oxytocin is implicated in the regulation of penile erection and yawning, and provide further evidence that oxytocin acts as a neuropeptide in the central nervous system.
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PMID:Oxytocin: an extremely potent inducer of penile erection and yawning in male rats. 379 49

Oxytocin (OT), vasopressin (AVP), and corticotropin (ACTH) levels were measured in peripheral plasma of male rats subjected to one of three models of stress: restraint, cold, or ether. ACTH secretion was increased in all three groups compared to unstressed controls. OT secretion was increased in rats subjected to restraint or ether but not cold. AVP secretion was increased only by ether stress. The data suggest that the hypothalamic and neurohypophysial contribution to the control of ACTH secretion may vary in response to different types of stress.
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PMID:Dissociation of oxytocin, vasopressin and corticotropin secretion during different types of stress. 608 65

Most neuropeptides are known to occur both in the central nervous system and in blood. This, as well as the occurrence of central nervous peptide effects after peripheral administration, show the importance of studying the relationships between the peptides in the two compartments. For many peptides, such as the enkephalins, TRH, somatostatin and MIF-1, poor penetration of the blood-brain barrier was shown. In other cases, including beta-endorphin and angiotensin, peptides are rapidly degraded during or just after their entry into brain or cerebrospinal fluid. Some peptides, such as insulin, delta-sleep-inducing peptide, and the lipotropin-derived peptides, enter the cerebrospinal fluid to a slight or moderate extent in the intact form. Many peptide hormones, such as insulin, calcitonin and angiotensin, act directly on receptors in the circumventricular organs, where the blood-brain barrier is absent. Oxytocin, vasopressin, MSH, and an MSH-analog alter the properties of the blood-brain barrier, which may result in altered nutritient supply to the brain. In conclusion, the diffusion of most peptides across the brain vascular endothelium seems to be severely restricted. There are, however, several alternative routes for peripheral peptides to act on the central nervous system. The blood-brain barrier is a major obstacle for the development of pharmaceutically useful peptides, as in the case of synthetic enkephalin-analogs.
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PMID:Minireview. Peptides and the blood-brain barrier. 630 42

An antibody raised against dynorphin 1-8 was immunoreactive in the rat neurohypophysis in vasopressin but not in oxytocin endings. Oxytocin but not vasopressin terminals were immunostained when a Met5-enkephalin, a N-terminally directed monoclonal beta-endorphin antibody and an enkephalin-Met5-Arg6-Phe7 antibody were applied. The immunocytochemical reactions indicate that oxytocin terminals and their granules store pro-enkephalin-A derived opioid peptide fragments.
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PMID:An attempt to characterize by immunocytochemical methods the enkephalin-like material in oxytocin endings of the rat neurohypophysis. 666 45

Histamine administered intraperitoneally increased, in a dose-dependent manner, AVP, OXT and PRL levels in plasma of rats, whereas alpha-MSH levels were not affected. Levels of AVP in plasma after histamine 20.0 mg/kg treatment were approximately 100-fold higher than those of controls, while OXT and PRL levels were approximately 7-fold higher after this treatment. CSF content of AVP, OXT, PRL and alpha-MSH was not influenced by histamine, indicating that a stimulated release of hormones from the pituitary into the blood is not accompanied by a concomitant increase of secretion of these hormones into the CSF. Convulsions induced by pentylenetetrazol were accompanied by a temporary increase in AVP levels and by strongly and consistently elevated OXT levels in plasma. PRL and alpha-MSH plasma levels were affected in a biphasic manner. A convulsion type 1 induced elevated PRL levels and diminished alpha-MSH levels, while a convulsion type 2 had no effect on plasma PRL concentration, but increased the concentration of alpha-MSH. Only the level of OXT in CSF was increased after a pentylenetetrazol-induced convulsion type 1. The present data suggest that histamine affects the release of AVP, while pentylenetetrazol might act more specifically on the OXT-releasing system. Furthermore, a possible relationship between the pentylenetetrazol-induced increase of OXT levels in the CSF and amnesia is suggested.
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PMID:Hypophyseal hormone levels in blood and cerebrospinal fluid in response to histamine and pentylenetetrazol. 715 99

The present study was undertaken to investigate whether beta-adrenoceptors are involved in regulation of yawning responses to oxytocin and alpha-melanocyte-stimulating hormone (alpha-MSH) in rats. Oxytocin administered intracerebroventricularly (ICV) at doses of 50 and 100 ng/rat elicited yawning. alpha-MSH (20 micrograms/rat, ICV) elicited not only yawning but also stretching and body shaking. RS-86 (2-ethyl-8-methyl-2,8-diazaspiro-(4,5)-decan-1,3-dion hydrobromide), a putative muscarinic M1 receptor agonist, administered ICV at a lower dose of 100 micrograms/rat and subcutaneously (SC) at doses of 0.25-2.5 mg/kg also elicited yawning. The yawning responses produced by these agents were markedly increased by intraperitoneal (IP) pretreatment with a beta-adrenoceptor antagonist, pindolol (20 mg/kg), which per se did not elicit yawning. The yawning induced by oxytocin (50 ng/rat, ICV) plus pindolol, but not that by alpha-MSH (20 micrograms/rat, ICV) or RS-86 (0.5 mg/kg, SC) plus pindolol, was inhibited by [d(CH2)5,Tyr(Me)2,Orn8]-vasotocin (100 ng/rat, ICV), an oxytocin receptor antagonist. The yawning induced by oxytocin, alpha-MSH, or RS-86 administered in combination with pindolol was inhibited by scopolamine (0.5 mg/kg, SC), a mucarinic receptor antagonist, without being affected by spiperone (0.5 mg/kg, SC), a dopamine D2 receptor antagonist. The results suggest that the yawning produced by the neuropeptides oxytocin and alpha-MSH is modulated by beta-adrenoceptor activity in an inhibitory manner as that produced by muscarinic M1 receptor agonists, and that it involves cholinergic, but not dopaminergic, activation.
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PMID:Involvement of beta-adrenoceptors in regulation of the yawning induced by neuropeptides, oxytocin and alpha-melanocyte-stimulating hormone, in rats. 761 71

The subfornical organ (SFO) was suggested to be the site of the central nervous system which mediates the stimulatory effect of angiotensin II (AII) on corticotropin (ACTH) release. To verify this hypothesis, ACTH response to peripherally administered AII was measured in rats with electrolytic lesion of the SFO. Increase in ACTH levels in response to AII (0.5 micrograms/kg or 2.0 micrograms/kg i.v. within 2 min) in conscious cannulated rats was dose-related and it was not affected by SFO lesion. The short infusion of AII (2.0 micrograms/kg) was enough to induce an elevation in plasma oxytocin. Oxytocin response to AII was reduced while that of aldosterone and blood pressure was not modified by SFO lesion. Our data show that an intact SFO is needed for a full response of oxytocin but not of ACTH release to peripherally injected AII.
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PMID:Angiotensin II induces reduced oxytocin but normal corticotropin release in rats with lesions of the subfornical organ. 772 Dec 31


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